Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.16.2 (PCP)
 3,761 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Long term environmental fate of polychlorinated dibenzo-p-dioxins (PCDD) and polychlorinated dibenzofurans (PCDF) were studied using the fugacity-based dynamic multimedia environmental fate model. New formulation about soil wind erosion into air was included into the model. Effect of process assumption, sensitivity analysis for parameters, and tentative validation against the measured sediment core analysis was performed. Mass fluxes between compartments were estimated by the dynamic modeling. From the model estimates, major mass fluxes coming from emission source were shown to go to the soil and water through wet/dry deposition, then go to degradation mainly in the soil and sediment. Major mass fluxes of TCDD and OCDD come from the impurities in CNP (Chlornitrofen) and PCP (Pentachlorophenol) directly into the soil. Consideration about multimedia environmental dynamics using the modeled mass fluxes was shown in the discussion.
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PMID:Simulation of long-term environmental dynamics of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans using the dynamic multimedia environmental fate model and its implication to the time trend analysis of dioxins. 1073 34

Mill process changes and source controls instituted in the late 1980s at pulp and paper mills along the British Columbia (BC) coast produced dramatic reductions in both the concentrations of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) and the TEQ (2,3,7,8-TCDD toxic equivalents). Nevertheless, questions remained as to whether the sediments were acting as contaminant sources or sinks, whether crab uptake pathways have stayed the same since the mills ceased producing PCDD/Fs, and whether improvement was faster at some sites than others. To examine the processes governing the changes in PCDD/F composition, PCDD/F sources and compositional trends for the coastal BC sites were interpreted using sediment and crab PCA (principal components analysis) models and two indices based on the three main groups of PCDD/Fs that covary in all PCA models. One index measured the relative inputs of chlorine bleaching PCDFs and PCP (pentachlorophenol)-related PCDDs at each mill and harbor site whereas the other measured the relative inputs of PCP wood preservatives and pulp mill effluents. Results indicated that PCDFs produced during chlorine bleaching accumulate from sediments to crabs more readily than the PCDDs but that the chlorine bleaching TCDFs have generally decreased in importance at all mill sites. In the years just before 1995, little change was observed in either the proportion of toxic 2,3,7,8-chlorinated congeners or the PCDD/F concentrations, and the improvements seemed to have largely ceased by 1995. The lack of change in PCA composition for the harbors provided a further, disturbing indication that ecosystem recovery may have stalled. Results also implied that the main route of PCDD/Fs into crabs shifted from uptake via a pelagic food web incorporating effluent-borne PCDD/Fs associated with suspended particulate matter to uptake via a benthic food web.
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PMID:Assessment of chlorinated dibenzo-p-dioxin and dibenzofuran trends in sediment and crab hepatopancreas from pulp mill and harbor sites using multivariate- and index-based approaches. 1202 64

Cultured rat hepatocytes were challenged with benzo[a]pyrene (BaP; 0.3-30 mum), naphthalene (NAPH; 0.1-100 mum), 2-methylnaphthalene (2-MNAPH; 0.1-100 mum), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; 0.001-1 nM), 2,3,7,8-tetrachlorodibenzofuran (TCDF; 0.005-5 nM) or pentachlorophenol (PCP; 0.1-100 mum) for 4-24 hr to define class-specific differences in hepatotoxic potential. Mitochondrial fragility and GSH status were monitored as indices of hepatocyte injury. A 4-hr challenge with BaP and PCP increased mitochondrial fragility in a concentration-dependent manner, while TCDD and TCDF elicited erratic increases, and NAPH and 2-MNAPH were without effect. Pretreatment of hepatocytes with 250 muM diamide enhanced the mitochondrial toxicity of BaP. The aryl hydrocarbon receptor agonists upregulated hepatocyte GSH levels by 24 hr, a response which in the case of BaP was preceded by varying degrees of GSH depletion between 6 to 16 hr. NAPH and 2-MNAPH transiently decreased hepatocyte GSH levels at 12 hr, but were without effect at later time points, while PCP did not modulate hepatocyte GSH levels. Modulation of hepatocyte GSH by BaP and TCDD was antagonized by 10 muM alpha-naphthoflavone. These data implicate oxidative mechanisms and aryl hydrocarbon receptor signalling in aromatic hydrocarbon hepatotoxicity.
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PMID:Cytotoxic response profiles of cultured rat hepatocytes to selected aromatic hydrocarbons. 2065 98

The cytotoxic responses of cultured rat renal cortico-tubular epithelial cells (TECs) and glomerular mesangial cells (GMCs) to selected polycyclic and polyhalogenated aromatic hydrocarbons (AHs) were evaluated to further define class specific differences in toxicity potential among these chemicals. Primary cultures of renal cells were exposed to benzo[a]pyrene (BaP, 0.3-30mum); naphthalene (NAPH, 1-1000mum); 2-methylnaphthalene (2-MNAPH, 1-1000mum), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, 0.01-1nm); 2,3,7,8-tetrachlorodibenzofuran (TCDF, 0.05-5nm; and pentachlorophenol (PCP, 0.1-10mum for 4 or 24hr. Measurements of mitochondrial membrane fragility in TECs revealed that the polycyclic aromatic hydrocarbons (PAHs) (BaP, NAPH and 2-MNAPH) preferentially injured these cells relative to halogenated aromatic hydrocarbons (HAHs). Extended exposures to all AHs tested were associated with moderate mitochondrial injury in TECs. Challenge of TECs with AHs for 4hr did not modulate GSH levels, although modest increases in this tripeptide occurred on extended exposures. Similar response profiles were observed in GMCs, where PAHs elicited mitochondrial damage by 4hr, while extended challenge was associated with injury in response to all AHs. Only aryl hydrocarbon receptor (AhR) ligands (BaP, TCDD and TCDF) depleted intracellular glutathione (GSH) in GMCs, while extended exposures to BaP and TCDD, as well as NAPH and 2-MNAPH, were associated with rebound increases in cellular GSH content. These data indicate that AHs can compromise renal cell function by interference with mitochondrial function and GSH homeostasis and implicate both epithelial and mesenchymal populations in the nephrotoxic response to this heterogeneous class of chemicals.
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PMID:Cytotoxic Response Profiles of Cultured Renal Epithelial and Mesenchymal Cells toSelected Aromatic Hydrocarbons. 2065 4

The present studies were conducted to assess cell-specific cytotoxic responses of the kidney to selected aromatic hydrocarbons (AHs) using in vitro culture systems of glomerular mesangial cells and cortical tubular epithelial cells. Primary cultures of glomerular mesangial cells or cortical tubular epithelial cells were treated for 24 hr with naphthalene (NAPH, 0.1-1000 mum), 2-methylnaphthalene (2-MNAPH, 0.1-1000 mum), benzo[a]pyrene (B[a]P, 0.3-300 mum), pentachlorophenol (PCP, 0.1-1000 mum), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, 0.001-1 nm) or 2,3,7,8-tetrachlorodibenzofuran (TCDF, 0.005-5 nm). [(3)H]Thymidine incorporation into DNA, cellular potassium content, and lactate dehydrogenase (LDH) leakage were used as indices of cytotoxicity. Glomerular mesangial cells exposed to NAPH or 2-MNAPH (0.1-1000 mum) exhibited [(3)H]thymidine incorporation profiles similar to those of the vehicle controls, whereas B[a]P at all concentrations and PCP at 1000 mum decreased [(3)H]thymidine incorporation in comparison with the controls. TCDD and TCDF increased [(3)H]thymidine incorporation relative to controls at 0.1 nm and 0.5 nm, respectively. Glomerular mesangial cells treated with NAPH or PCP exhibited decreased cellular potassium content and increased LDH leakage only at the 1000 mum concentration. In tubular epithelial cells, treatment with NAPH (10 or 1000 mum), 2-MNAPH (10 or 1000 mum), B[a]P (300 mum), and PCP (10 or 1000 mum) induced concentration-dependent decreases in [(3)H]thymidine incorporation relative to controls. In contrast, exposure of tubular epithelial cells to TCDD or TCDF did not modulate [(3)H]thymidine incorporation at any of the concentrations tested. A modest decrease in cellular potassium content and an increase in LDH leakage was observed at the 1000 mum concentration of PCP in tubular epithelial cells. On the basis of these data, we conclude that renal glomerular mesangial cells and tubular epithelial cells exhibit differential cytotoxic response profiles to AHs.
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PMID:Assessment of cell-specific cytotoxic responses of the kidney to selected aromatic hydrocarbons. 2069 83

The influence of soil composition (peat and clay content) on the leachability was investigated in batch leaching experiments for chemically diverse hydrophobic organic compounds (HOCs: PCP, PAHs, HCB, HCHs, PCBs, and TCDD/Fs). An experimental design was applied to generate 8 diverse soil matrices, and the results were evaluated by orthogonal projections to latent structures (OPLS), as well as compound specific response surface models. Overall, the distribution coefficients (logKd) of model HOCs were in the range of approx. 2.0-5.7. The Kd-values of HCHs, phenanthrene and PCP were positively correlated with the peat content. Kd-values of benzo(a)anthracene, HCB, and PCB 47 were positively correlated with both peat and clay content. The Kd-values of 1,3,6,8-TCDD and 1,3,6,8-TCDF were positively correlated with peat content but negatively correlated with clay content, while for PCB 153 and PCB 155 the correlations were reversed. The correlation between the Kd-values and the compounds' Kow-values was linearly for compounds with log Kow <6. For HOCs with log Kow>6, the Kd-values were leveling off, possibly due to small particles in the leachates. Our study demonstrated how complex interaction between both the organic matter and clay components influences the leachability of HOCs in a compound-specific manner.
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PMID:The influence of soil composition on the leachability of selected hydrophobic organic compounds (HOCs) from soils using a batch leaching test. 2358 46

The long-range transport potential (LRTP) and overall persistence (Pov) of 5 typical persisitent organic pollutants (POPs) through air and water in Poyang Lake were estimated by the TaPL3 model. The characteristic travel distance (CTD) and Pov of different POPs were compared. In addition, the key parameters were examined by the sensitivity analysis method using p, p'-DDT as an example. The results showed that the CTD(Air) of p, p'-DDT, gamma-HCH, HCB, PCP and 2, 3, 7, 8-TCDD ranged from 432 km (2, 3, 7, 8-TCDD) to 86 479 km (HCB), and the value of Pov(Air) ranged from 85.6 d (PCP) to 2 231 d (HCB), when POPs were emitted to the atmosphere. Soil phase was the main fate of these typical POPs, and it was about 72.0% percent of the total phase. Meanwhile, the CTD(Water) was from 4 207 km (PCP) to 1.19 x 10(5) km (gamma-HCH), and Pov(Water) was from 103 d (PCP) to 2 890 d (HCB), when POPs were emitted to the water. Sediment phase was the main fate of these typical POPs, and it was about 52.5% percent of the total phase. Half-life in the environment and octanol-water partition coefficient logarithm of POPs were the two main physical-chemical parameters that affected CTD and Pov. When compared with other similar studies in China, the CTD(Air) of related POPs in Poyang Lake is in the middle level. While the CTD(Water) was a little higher than other areas, which was due to the higher water depth and water flow velocity of Poyang Lake. Therefore, the higher water depth and water flow velocity were two significantly-affected parameters of CTD(Water). The results could provide a scientific basis to studies of environmental process and risks of POPs in Poyang Lake.
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PMID:[Simulation of long-range transport potential of POPs in Poyang Lake]. 2515 4